Methylprednisolone inhibits production of interleukin-1β and interleukin-6 in the spinal cord following compression injury in rats

Interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) are major inflammatory cytokines produced after spinal cord injury (SCI). This study sought to evaluate the effects of methylprednisolone (MP) on IL-1 beta and IL-6 protein in spinal cord tissue following SCI. Halothane-anesthetized, female Sprague-Dawley rats weighing (280-320 g) underwent laminectomy at T7-T8. No lesions were produced in animals, in the saline control and MP control groups. SCI was induced by temporary placement of an aneurysm clip at T7-T8, with a closing pressure of 55 g at the spinal level of T7-T8, resulting in spinal cord compression for one minute. Animals with SCI were treated with NIP (30 mg/kg sc) or an equal volume of saline. IL-1 beta and IL-6 spinal cord protein were measured by enzyme-linked immunosorbent assays (ELISA). Data were summarized as mean +/- SD and compared by two-way analysis of variance (ANOVA). IL-1 beta and IL-6 levels were elevated in the SCI + Saline animals (P < 0.01) compared with saline control, MP control, and SCI + MP-treated animals. The rise in IL-1 beta and IL-6 levels after SCI was blunted after administration of MP, suggesting an interaction between glucocorticosteroids and the cytokine cascade after spinal cord trauma. Further evaluation of the effects of NIP on the cytokine cascade may be important in assessing whether or not the anti-inflammatory effects of glucocorticosteroids confer neuroprotection after SCI.